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Background and Aim: Filarial infections affect over 150 million people in the tropics. One of the major forms of filarial pathologies is lymphedema; a condition where the immune response is significantly altered, resulting in changes in the normal flora. Staphylococcus hominis, a human skin commensal, can also be pathogenic in immunocompromised individuals. Therefore, there is the possibility that S. hominis could assume a different behavior in filarial lymphedema patients. To this end, we investigated the levels of antibiotic resistance and extent of mecA gene carriage in S. hominis among individuals presenting with filarial lymphedema in rural Ghana. Method: We recruited 160 individuals with stages I-VII lymphedema, in a cross-sectional study in the Ahanta West District of the Western Region of Ghana. Swabs from lymphedematous limb ulcers, pus, and cutaneous surfaces were cultured using standard culture-based techniques. The culture isolates were subjected to Matrix-Assisted Laser Desorption/Ionization Time of Flight (MALDI-TOF) mass spectrometry for bacterial identification. Antimicrobial susceptibility testing (AST) was performed using the Kirby-Bauer method. mecA genes were targeted by polymerase chain reaction for strains that were cefoxitin resistant. Results: In all, 112 S. hominis were isolated. The AST results showed resistance to chloramphenicol (87.5%), tetracycline (83.3%), penicillin (79.2%), and trimethoprim/sulphamethoxazole (45.8%). Of the 112 strains of S. hominis, 51 (45.5%) were resistant to cefoxitin, and 37 (72.5%) of the cefoxitin-resistant S. hominis haboured the mecA gene. Conclusion: This study indicates a heightened level of methicillin-resistant S. hominis isolated among filarial lymphedema patients. As a result, opportunistic infections of S. hominis among the already burdened filarial lymphedema patients in rural Ghana may have reduced treatment success with antibiotics.
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Background: Lymphatic Filariasis (LF), a neglected tropical disease, has been speculated to be complicated by secondary bacteria, yet a systematic documentation of these bacterial populations is lacking. Thus, the primary focus of this study was to profile bacteria diversity in the progression of filarial lymphedema among LF individuals with or without wounds. Methods: A cross-sectional study design recruited 132 LF individuals presenting with lymphedema with or without wounds from eight communities in the Ahanta West District in the Western Region, Ghana. Swabs from the lymphedematous limbs, ulcers, pus, and cutaneous surfaces were cultured using standard culture-based techniques. The culture isolates were subsequently profiled using Matrix-assisted Laser Desorption/Ionization Time of Flight Mass Spectrometry. Results: Of the 132 LF participants recruited, 65% (85) had filarial lymphedema with no wounds. In total, 84% (235) of the bacterial isolates were identified. The remaining 16% (46) could not be identified with the method employed. Additionally, 129(55%) of the strains belonged to the phylum Firmicutes, while 61 (26%) and 45 (19%) represented Proteobacteria and Actinobacteria, respectively. Generally, irrespective of the samples type (i.e., wound sample and non-wound samples), there was a sharp increase of bacteria diversity from Stages 1 to 3 and a drastic decrease in these numbers by Stage 4, followed by another surge and a gradual decline in the advanced stages of the disease. The Shannon Diversity Index and Equitability for participants with and without wounds were (3.482, 0.94) and (3.023, 0.75), respectively. Further, Staphylococcus haemolyticus and Escherichia coli showed resistance to tetracycline, chloramphenicol, and penicillin. Conclusion: The present study reveals a sharp decline in bacterial load at the late stages of filarial lymphedema patients. In addition, we report an emerging antimicrobial resistance trend of S. haemolyticus and E. coli against commonly used antibiotics such as tetracycline, chloramphenicol, and penicillin in communities endemic for LF in the Ahanta West District, Ghana. This could pose a huge challenge to the management of the disease; particularly as current treatments are not quite effective against the infection.
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Objective: To determine causes of visual impairment (VI) among staff of the Eye Centre at the Korle Bu Teaching Hospital. Design: This was a cross-sectional study. Setting: The Eye Centre, Korle Bu Teaching Hospital (KBTH), from October 2016 to March 2017 on all consenting members of staff. Participants: Eighty-four (79.3%) of 106 consenting staff members participated in this study. Data collection/Intervention: A detailed history (demographic, ocular, medical co-morbid conditions), ocular examination and relevant diagnostic investigations were conducted. Interventions initiated included treatment for glaucoma, dry eye and allergic conjunctivitis and spectacles prescription for refractive errors. Main outcomes: Prevalence of avoidable causes of VI (glaucoma, cataract, refractive errors). Secondary outcomes included prevalence of unavoidable causes of VI. Results: Eighty-four (79.3%) members of staff participated in this study. Most of the participants were females, 54(64.3 %). Age ranged from 23 to 60 years with an average of 35.8±9.9 years (mean ± SD).Prevalence of VI was 9.5 % (8/84), all due to uncorrected refractive error. Other known causes of VI included open angle glaucoma in 12(14.3 %), macular scar of unknown cause, 1(1.2 %) and sutural cataract, 1(1.2 %) but were all visually insignificant. Conclusions: The prevalence of VI among the staff of the Eye Centre of the KBTH was 9.5 %, all due to refractive errors. Other known causes of avoidable visual impairment and blindness encountered were glaucoma (14.3 %), macular scar (1.2 %) and cataract (1.2 %), all asymptomatic. Routine eye screening should be part of periodic medical examination for employees. Funding: None declared.